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过氧化物酶体增殖物激活受体(PPARs)对巨噬细胞激活和功能的调控。

Control of macrophage activation and function by PPARs.

机构信息

Division of Endocrinology, Metabolism and Gerontology, Department of Medicine, Stanford University School of Medicine, Stanford, CA 94305-5103, USA.

出版信息

Circ Res. 2010 May 28;106(10):1559-69. doi: 10.1161/CIRCRESAHA.110.216523.

Abstract

Abstract: Macrophages, a key component of the innate defense against pathogens, participate in the initiation and resolution of inflammation, and in the maintenance of tissues. These diverse and at times antithetical functions of macrophages are executed via distinct activation states, ranging from classical to alternative to deactivation. Because the dysregulation of macrophage activation is pathogenically linked to various metabolic, inflammatory and immune disorders, regulatory proteins controlling macrophage activation have emerged as important new therapeutic targets. Here, the mechanisms by which peroxisome proliferator-activated receptors (PPARs) transcriptionally regulate macrophage activation in health and disease states, including obesity, insulin resistance and cardiovascular disease, are reviewed.

摘要

摘要

巨噬细胞是先天防御病原体的关键组成部分,参与炎症的启动和消退以及组织的维持。巨噬细胞的这些不同且有时相反的功能是通过不同的激活状态来执行的,从经典到替代到失活。由于巨噬细胞激活的失调与各种代谢、炎症和免疫紊乱有关,因此控制巨噬细胞激活的调节蛋白已成为重要的新治疗靶点。本文综述了过氧化物酶体增殖物激活受体 (PPARs) 在健康和疾病状态(包括肥胖、胰岛素抵抗和心血管疾病)下转录调控巨噬细胞激活的机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebe8/2897247/65c5c0c5d6f6/nihms198853f1.jpg

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本文引用的文献

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Macrophages, inflammation, and insulin resistance.巨噬细胞、炎症与胰岛素抵抗。
Annu Rev Physiol. 2010;72:219-46. doi: 10.1146/annurev-physiol-021909-135846.
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Nat Rev Immunol. 2008 Dec;8(12):958-69. doi: 10.1038/nri2448.
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Mechanisms of macrophage activation in obesity-induced insulin resistance.肥胖诱导的胰岛素抵抗中巨噬细胞活化的机制。
Nat Clin Pract Endocrinol Metab. 2008 Nov;4(11):619-26. doi: 10.1038/ncpendmet0976. Epub 2008 Oct 7.

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